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作 者:Qi Zhang Jiancan Du Xiao Han Yanru Hu
机构地区:[1]CAS Key Laboratory of Tropical Plant Resources and Sustainable Use,Xishuangbanna Tropical Botanical Garden,Chinese Academy of Sciences,Kunming,Yunnan 650223,China [2]College of Life Sciences,University of Chinese Academy of Sciences,Beijing 100049,China [3]College of Biology,State Key Laboratory of Chemo/Biosensing and Chemometrics,Hunan Province Key Laboratory of Plant Functional Genomics and Developmental Regulation,Hunan University,Changsha 410082,China
出 处:《Plant Diversity》2024年第6期791-803,共13页植物多样性(英文版)
基 金:supported by the Natural Science Foundation of China(32270613,31922009,and 31870259);the Yunnan Fundamental Research Projects(202201AS070051,202001AV070009,2019FI006,202001AT070118,and 202101AW070005,202401AT070220);the CAS“Light of West China”Program(to X.H.);the Youth Innovation Promotion Association of the of Chinese Academy of Sciences(Y201973 and 2022399).
摘 要:Salinity is a severe abiotic stress that affects plant growth and yield.Salinity stress activates jasmonate(JA)signaling in Arabidopsis thaliana,but the underlying molecular mechanism remains to be elucidated.In this study,we confirmed the activation of JA signaling under saline conditions and demonstrated the importance of the CORONATINE INSENSITIVE1(COI1)-mediated JA signaling for this process.Phenotypic analyses reflected the negative regulation of JASMONATE ZIM-DOMAIN(JAZ)repressors during salinity stress-enhanced JA signaling.Mechanistic analyses revealed that JAZ proteins physically interact with ABSCISIC ACID-RESPONSIVE ELEMENT BINDING FACTOR1(ABF1),AREB1/ABF2,ABF3,and AREB2/ABF4,which belong to the basic leucine zipper(bZIP)transcription factor family and respond to salinity stress.Analyses on the ABF3 overexpression plants and ABF mutants indicated the positive role of ABF3 in regulating JA signaling under saline condition.Furthermore,ABF3 overexpression partially recovered the JA-related phenotypes of JAZ1-D3A plants.Moreover,ABF3 was observed to indirectly activate ALLENE OXIDE SYNTHASE(AOS)transcription,but this activation was inhibited by JAZ1.In addition,ABF3 competitively bind to JAZ1,thereby decreasing the interaction between JAZ1 and MYC2,which is the master transcription factor controlling JA signaling.Collectively,our findings have clarified the regulatory effects of ABF3 on JA signaling and provide new insights into how JA signaling is enhanced following an exposure to salinity stress.
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